Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Downregulation of Scd1 promotes cardiac reprogramming by enhancing mitochondrial metabolism through PGC1α

ABSTRACT: Direct cardiac reprogramming of fibroblasts into induced cardiac-like myocytes (iCMs) has emerged as a promising therapeutic strategy to remuscularize injured myocardium. However, the intrinsic metabolic demands that drive the iCM program and maturity remain unclear. Here, we induce efficient iCM production and maturation through metabolic pathway modulations. We show that the knockdown of Stearoyl-CoA desaturase 1 (Scd1) facilitates cardiac reprogramming and functional maturation of iCM. Through Bulk-RNAseq analysis, we found that compared with control group, fibrosis and inflammatory response pathway were significantly down-regulated, while cardiac related features and fatty acid metabolism related genes were up-regulated in shscd1 group. We further observed the expression level of PGC1α which serves as a master regulator of mitochondrial biogenesis and function was significantly increased in shScd1 group from RNA-seq. Mechanistically, we proved that Scd1 knockdown activates PGC1α/PPARβ transcription signal, which further promotes cardiac reprogramming, and induced cardiomyocytes demonstrated more frequent beating, calcium oscillation, and higher energy metabolism as evidenced by increased mitochondrial respiration and gene expression associated with FAO, which provides a new strategy and theoretical basis for cardiac regeneration and repair

ORGANISM(S): Mus musculus

PROVIDER: GSE271439 | GEO | 2025/04/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Downregulation of Scd1 promotes cardiac reprogramming by enhancing mitochondrial metabolism through PGC1α [RNA-seq]

Project description:Direct cardiac reprogramming of fibroblasts into induced cardiac-like myocytes (iCMs) has emerged as a promising therapeutic strategy to remuscularize injured myocardium. However, the intrinsic metabolic demands that drive the iCM program and maturity remain unclear. Here, we induce efficient iCM production and maturation through metabolic pathway modulations. To explore the metabolic heterogeneity of iCMs, we performed single cell RNA sequencing (scRNA-seq) at reprograming day 14. Using single-cell metabolic flux estimation and flux balance analysis on day 14 iCM, we characterized the metabolic heterogeneity of iCMs and identified fatty acid oxidation (FAO) as a critical factor in iCM conversion. Mechanistically, we proved that Scd1 knockdown activates PGC1α/PPARβ transcription signal, which further promotes cardiac reprogramming, and induced cardiomyocytes demonstrated more frequent beating, calcium oscillation, and higher energy metabolism as evidenced by increased mitochondrial respiration and gene expression associated with FAO, which provides a new strategy and theoretical basis for cardiac regeneration and repair. Our findings collectively highlight FAO as a key determinant of iCM fate and offer new therapeutic avenues for advancing reprogramming strategies.

2025-04-23 | GSE285211 | GEO

Downregulation of Scd1 promotes cardiac reprogramming by enhancing mitochondrial metabolism through PGC1α

Project description:Downregulation of Scd1 promotes cardiac reprogramming by enhancing mitochondrial metabolism through PGC1α

| PRJNA1131397 | ENA

Downregulation of Scd1 promotes cardiac reprogramming by enhancing mitochondrial metabolism through PGC1α [RNA-seq]

Project description:Downregulation of Scd1 promotes cardiac reprogramming by enhancing mitochondrial metabolism through PGC1α [RNA-seq]

| PRJNA1201855 | ENA

Expression data of A939572 SCD1 inhibitor treated ccRCC cells

Project description:Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. In order to understand the mechanism by which the SCD1 inhibitor mediated its anti-tumor effects, we performed gene array analysis and compared expression patterns between treated and untreated samples. Four established ccRCC cell lines purchased from ATCC were treated with DMSO control versus A939572 over a 24 hour time period. RNA from each group was isolated and sent of for gene array anaylsis. Gene expression data from each individual treatment group was normalized to its respective DMSO contol, and resulting expression patterns associated with drug exposure was compared between the four cell lines.

2012-10-11 | E-GEOD-41485 | biostudies-arrayexpress

SCD1

Project description:Arabidopsis thaliana SCD1, SCD1 [Source:UniProtKB/TrEMBL;Acc:A0A178WQS8], is differentially expressed in 51 experiment(s);

| AT1G49040 | ExpressionAtlas

scd1

Project description:Schizosaccharomyces pombe scd1, RhoGEF Scd1 [Source:PomBase;Acc:SPAC16E8.09], is differentially expressed in 1 experiment(s);

| SPAC16E8.09 | ExpressionAtlas

SCD1

Project description:Arabidopsis thaliana SCD1, SCD1 [Source:UniProtKB/TrEMBL;Acc:A0A178WQS8], is expressed in 16 baseline experiment(s);

| AT1G49040 | ExpressionAtlas

Expression data in HCT-116 colon cancer cell treated with SCD1 inhibitor or in SCD1 knocked out HCT-116 cell

Project description:To understand molecular mechanisms underlying the growth inhibitory ativity of Stearoyl-CoA desaturase-1 (SCD1) inhibitor, we performed microarray analysis using HCT-116 colorectal cancer cells, in which SCD1 was pharmacologically blocked or genetically ablated.

2017-08-01 | GSE98364 | GEO

SCD1 Modulates the Skin Homeostasis via Sustaining Hemidesmosomes

Project description:Niche for stem cells can profoundly influence the position and fate of stem cells in tissue homeostasis and associated disorders, however, the mechanisms underlying the maintenance of stem cell niche remain poorly understood. Here we report that fatty acid desaturation catabolized by stearoyl-coenzyme A desaturase 1 (SCD1) regulates the activity of hair follicle stem cells (HFSCs) via blocking the formation of the bulge, a niche for HFSCs. We further unraveled that the abnormal hair growth in mice with SCD1 deletion is due to its function in K14+ basal keratinocytes rather than directly affecting HFSCs. Mechanistically, SCD1 deficiency impaired the expression of integrin α6 and the formation of hemidesmosomes (HDs), and thus allowed the activation of FAK in K14+ keratinocytes. Activated FAK subsequently stimulated PI3K and promoted the differentiation and proliferation of these keratinocytes, resulting in downward extension of the outer root sheath (ORS) and the disruption of bulge formation. Interestingly, inhibition of PI3K signaling restored bulge formation and normalized HFSCs and hair growth. Supplementation of oleic acid, the product of SCD1, to SCD1-/- mice also enhanced HD numbers, normalized the niche of HFSCs, and promoted hair growth in SCD1-/- mice. Taken together, SCD1 is indispensable for hair growth through stabilizing the number of HDs and thus sustaining bulge formation for HFSC residence and periodic activity.

2023-02-08 | GSE184346 | GEO

Scd1 Knockout Mice on very low fat diet

Project description:Stearoyl-CoA desaturase 1-deficient (SCD1-/-) mice have impaired monounsaturated fatty acid (MUFA) synthesis. When maintained on a very low-fat, high-carbohydrate (VLF-HC) diet, SCD1-/- mice develop severe hypercholesterolemia characterized by an increase in apolipoprotein B-containing lipoproteins and the appearance of lipoprotein-X. Additionally, high-density lipoprotein cholesterol is dramatically reduced in VLF-HC SCD1-/- mice. The concomitant presence of elevated plasma bile acids, bilirubin and aminotransferases in the VLF-HC SCD1-/- mouse are indicative of hepatic dysfunction. Supplementation of the VLF-HC diet with unsaturated fat (canola oil), but not saturated fat (coconut oil), prevents these plasma phenotypes. However, dietary oleate was not as effective as canola oil in reducing low-density lipoprotein cholesterol, signifying an additional role for dietary polyunsaturated fatty acid deficiency in the development of this phenotype. These results indicate that lack of SCD1 results in an increased requirement for dietary unsaturated fat to compensate for impaired MUFA synthesis and to prevent hypercholesterolemia and hepatic dysfunction. Keywords: repeat (genotype and diet)

2005-12-23 | GSE3889 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data